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1 ie Kinder der Tuberkuloesen (Children of the Tuberculous).
2 illi in the lung and spleen after a virulent tuberculous aerosol challenge.
3  fluid and plasma to differentially diagnose tuberculous and malignant pleural effusion.
4                              Recovery of the tuberculous and nontuberculous isolates by the Tween 80-
5                              Recovery of the tuberculous and nontuberculous mycobacteria following CB
6 trument-negative MGIT cultures included both tuberculous and nontuberculous mycobacteria.
7 ell surface molecules present in several non-tuberculous and opportunistic mycobacterial species.
8                                              Tuberculous and postoperative infections were excluded.
9 entify and differentiate between features of tuberculous and pyogenic spondylodiscitis on MR images.
10                 Mortality from pneumococcal, tuberculous, and culture-negative meningitis was high in
11 es of lymph node cells from protein-deprived tuberculous animals.
12 centrations of rifampicin, a first-line anti-tuberculous antibiotic targeting RNA polymerase.
13  Their intriguing conservation in pathogenic tuberculous bacteria and the fact that these highly immu
14 , serofibrinous, and fungoid forms), whereas tuberculous bursitis exhibited two patterns of involveme
15 ree cows, 3 Mycobacterium bovis BCG-infected tuberculous cattle, or 3 cows artificially inoculated wi
16 5B-immunized mice (305 +/- 9 days) after the tuberculous challenge was extended 102 days relative to
17 eting cells, and significant resistance to a tuberculous challenge.
18 okines in PTB individuals at the end of anti-tuberculous chemotherapy (ATT).
19 escribes a novel PPD protein present only in tuberculous complex mycobacteria.
20  contribute to the granulomatous response in tuberculous diseases.
21 of DILI were acetaminophen (35.0 %) and anti-tuberculous drugs (34.7 %).
22 hat cares for about 200 patients with active tuberculous each year.
23 t include background immunity induced by non-tuberculous environmental mycobacteria, diversity of BCG
24                                       In the tuberculous granulation tissue surrounding caseous and l
25 ives: To ascertain the 3D shape of the human tuberculous granuloma and its spatial relationship with
26 sential for maintaining the structure of the tuberculous granuloma and may regulate the granulomatous
27                Thus, TNF is not required for tuberculous granuloma formation, but maintains granuloma
28 t and consequences of vascularization of the tuberculous granuloma in the zebrafish-Mycobacterium mar
29 , and IL-35-producing B cells infiltrated to tuberculous granuloma of patients with ATB.
30 TNF results in marked disorganization of the tuberculous granuloma, as demonstrated by the dissolutio
31 gs about the composition and dynamics of the tuberculous granuloma, the central host structure in myc
32 n, and are amplified and disseminated by the tuberculous granuloma.
33 cted macrophages undergoing apoptosis in the tuberculous granuloma.
34 erates macrophage recruitment to the forming tuberculous granuloma.
35 le in modulating the cellular composition of tuberculous granuloma; 2) CXCR3 impairs antimycobacteria
36                 What is happening inside the tuberculous granuloma?
37 is essential for the formation of protective tuberculous granulomas and regulates the expression of o
38 he observed patterns of neutrophils in human tuberculous granulomas and the susceptibility of humans
39                                              Tuberculous granulomas have long been considered host-pr
40 this probe to evaluate the oxygen tension in tuberculous granulomas in four animal models of disease:
41 eity of local immunologic characteristics of tuberculous granulomas in nonhuman primates.
42 Immunity, Egen et al. present live images of tuberculous granulomas of the mouse, demonstrating the i
43                                    Zebrafish tuberculous granulomas undergo caseous necrosis, similar
44 e functional consequences of angiogenesis in tuberculous granulomas, and data that balanced inflammat
45 tly elevated in the inflammatory zone of the tuberculous granulomas, and in the nongranulomatous pneu
46 le in both the construction and breakdown of tuberculous granulomas, our results suggest that TDM may
47 rious conditions postulated to be operant in tuberculous granulomas, suggesting that their granuloma-
48                                     Although tuberculous granulomas, which are composed of infected m
49                     In contrast to mammalian tuberculous granulomas, zebrafish lesions contain few ly
50 ing persistence in mycobacteria-which models tuberculous granulomas-are partly determined by a mechan
51 s undergo caseous necrosis, similar to human tuberculous granulomas.
52 he functional capacity of these cells within tuberculous granulomas.
53 d NO are present in specialized areas of the tuberculous granulomas; their precise role in human TB r
54               Since apoptosis is observed in tuberculous granulomata, we investigated the molecular m
55                                Malnourished, tuberculous guinea pigs harbored only 20 and 60% of the
56 Hepatobiliary tuberculosis includes miliary, tuberculous hepatitis or localized forms.
57 p insights into different layers of the anti-tuberculous immune response and the identification of im
58 individuals who had radiographic evidence of tuberculous infection (i.e., calcified granulomas) were
59  the contributions of reactivation of latent tuberculous infection (LTBI) and the progression of new
60 tor from such countries increase the risk of tuberculous infection among young children.
61 veillance data concerning groups at risk for tuberculous infection and allows recommended public heal
62 mportant measures for interpreting trends in tuberculous infection and disease but are complicated by
63 itis C and graft failure without evidence of tuberculous infection at death.
64  the age-stratified prevalence difference of tuberculous infection between case and control networks,
65                       Reactivation of latent tuberculous infection by aminoguanidine treatment was co
66 t RNI are required for the control of murine tuberculous infection caused by both laboratory and clin
67                           The annual risk of tuberculous infection for white men in the United States
68 To assess whether there is increased risk of tuberculous infection in children who traveled to or had
69                               The outcome of tuberculous infection in mice deficient in the CD11b sub
70 nd incentive approaches, treatment of latent tuberculous infection in those HIV-seropositive, and scr
71 tion-based national data are available about tuberculous infection in young people from such backgrou
72  is not useful in screening for asymptomatic tuberculous infection or for diagnosing active tuberculo
73                                    A case of tuberculous infection was defined as a positive tubercul
74                             The incidence of tuberculous infection was measured in a cohort of 8809 c
75 mechanisms involved in the control of latent tuberculous infection were examined using two murine exp
76                 In an at-risk population for tuberculous infection who were either tuberculin skin te
77 are important for containing and restricting tuberculous infection, and suggest that malnutrition-ind
78             In a setting with a high risk of tuberculous infection, HIV-1 increases the risk of recur
79   The secondary outcome was the incidence of tuberculous infection, measured using tuberculin skin te
80 importance of Th1 immunity in the control of tuberculous infection, the results of the present study
81 p with a high prevalence of tuberculosis and tuberculous infection, these efforts remain an important
82 cines in cattle, a natural target species of tuberculous infection.
83 morphological features with persistent human tuberculous infection.
84 city of the test depended on the presence of tuberculous infection.
85 phage activation in controlling a persistent tuberculous infection.
86 ar cells from persons across the spectrum of tuberculous infection.
87 ity has a high positive predictive value for tuberculous infection.
88 tified by country and baseline prevalence of tuberculous infection: group 1 strengthened tuberculosis
89  critical to the pathogenesis of progressive tuberculous infections in animal models.
90  on disease progression in mice with chronic tuberculous infections.
91 tral role that CD4 cells play in controlling tuberculous infections.
92  the host in both persistent and reactivated tuberculous infections.
93  this therapeutic approach markedly inhibits tuberculous inflammation in lungs, increases the surviva
94 smigration across pleural mesothelium during tuberculous inflammation was investigated.
95                              Recovery of the tuberculous isolates following NALC-NaOH processing aver
96 are as follows: growth of MDR TB from an old tuberculous lesion in a patient who was never treated fo
97                Liquefaction of solid caseous tuberculous lesions and the subsequent cavity formation
98                     Paradoxical expansion of tuberculous lesions during therapy should be treated wit
99 PSMA PET-positive lung cancers as well as in tuberculous lesions from our histologic database.
100 ism, drug penetration, and immune control of tuberculous lesions has the potential to facilitate drug
101                       Advances in monitoring tuberculous lesions have utilized the common glucoside [
102 both macrophage physiology and the nature of tuberculous lesions in man and animals suggests that hyp
103                                        The 2 tuberculous lesions showed an SUVmax of 7.8 and 2.5.
104  lymphocytes and immature macrophages in the tuberculous lung are basic to the local immunopathogenes
105 found in the affected but not the unaffected tuberculous lung compared with healthy controls.
106 ons associated with B cell-rich foci seen in tuberculous lung granulomas.
107 F-alpha) was also significantly increased in tuberculous lungs and was principally localized to the n
108  the 3D microanatomical environment of human tuberculous lungs by using micro computed tomography, hi
109 e in controlling TB, its expression in human tuberculous lungs has not been systematically characteri
110                                              Tuberculous lymphadenitis (TBL) is the most common form
111 inal failure, mutations in the NOD2 gene and tuberculous lymphadenitis has not been described before.
112                                              Tuberculous lymphadenitis is the main manifestation of e
113 evidence proved or was highly suggestive for tuberculous lymphadenitis.
114  in 2002 will have prevented 29,729 cases of tuberculous meningitis (5th-95th centiles, 24,063-36,192
115 e cerebrospinal fluid (CSF) of patients with tuberculous meningitis (TBM) are associated with TBM-IRI
116                 Mortality and morbidity from tuberculous meningitis (TBM) are common, primarily due t
117                      Point-of-care tests for tuberculous meningitis (TBM) are needed.
118        Pretreatment predictors of death from tuberculous meningitis (TBM) are well established, but w
119  a fully automated PCR assay, as the initial tuberculous meningitis (TBM) diagnostic test.
120                             Murine models of tuberculous meningitis (TBM) have not reflected the seve
121 ome, and prognostic factors in children with tuberculous meningitis (TBM) in Europe are limited.
122                                              Tuberculous meningitis (TBM) is a devastating form of tu
123                                              Tuberculous meningitis (TBM) is a devastating infection
124                                              Tuberculous meningitis (TBM) is a frequent cause of meni
125                                              Tuberculous meningitis (TBM) is a severe complication of
126                             The diagnosis of tuberculous meningitis (TBM) is difficult and poses a si
127                               Drug-resistant tuberculous meningitis (TBM) is difficult to diagnose an
128                                              Tuberculous meningitis (TBM) is the most devastating for
129                                              Tuberculous meningitis (TBM) is the most lethal form of
130                                              Tuberculous meningitis (TBM) is the most severe form of
131                                              Tuberculous meningitis (TBM) is the most severe form of
132                                              Tuberculous meningitis (TBM) leads to death or disabilit
133                     The delayed diagnosis of tuberculous meningitis (TBM) leads to poor outcomes, yet
134 ulosis load in the brain of individuals with tuberculous meningitis (TBM) may reflect the host's abil
135                Neurological complications of tuberculous meningitis (TBM) often lead to raised intrac
136 noassay) in cerebral spinal fluid (CSF) from tuberculous meningitis (TBM) patients.
137                                              Tuberculous meningitis (TBM) remains a major cause of de
138                               Mortality from tuberculous meningitis (TBM) remains around 30%, with mo
139                                              Tuberculous meningitis (TBM) research is hampered by low
140             Early diagnosis and treatment of tuberculous meningitis (TBM) saves lives, but current la
141  a national molecular diagnostic service for tuberculous meningitis (TBM) using an in-house IS6110-ta
142 ibute to the high morbidity and mortality of tuberculous meningitis (TBM), but the link between infla
143 s reported as a common complication in adult tuberculous meningitis (TBM), yet few studies have syste
144 udy of HIV-infected, ART-naive patients with tuberculous meningitis (TBM).
145 l fluid (CSF) inflammation, and outcome from tuberculous meningitis (TBM).
146 e available on their use in the diagnosis of tuberculous meningitis (TBM).
147 one is recommended as adjunctive therapy for tuberculous meningitis (TBM).
148 flammatory therapies may improve outcomes in tuberculous meningitis (TBM).
149 High-dose rifampicin may improve outcomes of tuberculous meningitis (TBM).
150 is evaluated in novel treatment regimens for tuberculous meningitis (TBM).
151                                              Tuberculous meningitis (TM) is difficult to diagnose and
152 diagnosis; the rest had probable or possible tuberculous meningitis according to published criteria.
153                  We calculated the number of tuberculous meningitis and miliary tuberculosis cases th
154 consistently high efficacy against childhood tuberculous meningitis and miliary tuberculosis, but var
155  The polymorphisms were associated with both tuberculous meningitis and pulmonary tuberculosis and we
156 lware discusses the challenges of diagnosing tuberculous meningitis and the implications of the study
157 ants were classified as probable or definite tuberculous meningitis by uniform case definition, exclu
158                 Consequently, differences in tuberculous meningitis characteristics across the lifesp
159 rospinal fluid of humans with HIV-associated tuberculous meningitis commonly express surface OX40 pro
160 87; 16 of 23 cases) for probable or definite tuberculous meningitis compared with 43% (23-66; 10/23)
161 uman immunodeficiency virus (HIV)-associated tuberculous meningitis despite limited data supporting t
162 6 in cerebrospinal fluid leukocytes improves tuberculous meningitis diagnosis.
163                                              Tuberculous meningitis disproportionately affects young
164                                Children with tuberculous meningitis had baseline magnetic resonance i
165                 Despite treatment, childhood tuberculous meningitis has very poor outcomes.
166 00) children younger than 15 years developed tuberculous meningitis in 2019.
167         With composite standard, we detected tuberculous meningitis in 22 (17%) of 129 participants.
168                      Laboratory evidence for tuberculous meningitis is difficult to acquire due to th
169                                              Tuberculous meningitis is especially common in young chi
170 ing the care of critically ill patients with tuberculous meningitis is poor and many patients do not
171                                              Tuberculous meningitis is the most severe form of tuberc
172 design in Vietnam with cases that had either tuberculous meningitis or pulmonary tuberculosis.
173                     Advances in the field of tuberculous meningitis predominantly focus on diagnosis,
174 logical differences adults and children with tuberculous meningitis receive similar treatment and are
175 search that were drafted at an international tuberculous meningitis research meeting organized by the
176 ematic review and meta-analysis of childhood tuberculous meningitis studies published up to Oct 12, 2
177 and low threshold for empirical treatment of tuberculous meningitis suspects.
178 ION: Xpert Ultra detected significantly more tuberculous meningitis than did either Xpert or culture.
179  higher rate of survival among patients with tuberculous meningitis than standard treatment.
180 apeutic, and neurosurgical interventions for tuberculous meningitis that will improve morbidity and m
181               Here, we use a rabbit model of tuberculous meningitis to evaluate the severity of disea
182                                              Tuberculous meningitis was observed in animals given M.
183 o hundred and eighty patients with suspected tuberculous meningitis were enrolled.
184 usly reported that rabbits with experimental tuberculous meningitis were protected from death by a co
185 fluid specimens from patients with suspected tuberculous meningitis were stained by conventional Zieh
186 infected adults with a clinical diagnosis of tuberculous meningitis who were admitted to one of two V
187               Among the 24 000 children with tuberculous meningitis, 16 100 (14 900-17 300) were esti
188                          The pathogenesis of tuberculous meningitis, a devastating complication of tu
189               Among HIV-positive adults with tuberculous meningitis, adjunctive dexamethasone, as com
190 coccal meningitis, 48 with culture-confirmed tuberculous meningitis, and 2900 with culture-negative C
191 gitis, 46% (22 of 48) and 56% (27 of 48) for tuberculous meningitis, and 41% (1181 of 2900) and 49% (
192 ents with culture-confirmed pneumococcal and tuberculous meningitis, and all patients with culture-ne
193 t approaches to prevent, diagnose, and treat tuberculous meningitis, and there are still too few answ
194 le tuberculous meningitis, three as possible tuberculous meningitis, and two as not tuberculous menin
195 d the prevalence of cryptococcal meningitis, tuberculous meningitis, bacterial meningitis, and cerebr
196 gher rifampicin doses may improve outcome of tuberculous meningitis, but the desirable exposure and n
197                           Among persons with tuberculous meningitis, no evidence of beneficial effect
198  hyponatraemia, which frequently accompanies tuberculous meningitis, remain to be elucidated.
199 ds are recommended as adjunctive therapy for tuberculous meningitis, the mechanism underlying their b
200                                           In tuberculous meningitis, the polymorphism is associated w
201 se eight, three were categorised as probable tuberculous meningitis, three as possible tuberculous me
202                      Using a rabbit model of tuberculous meningitis, we evaluated the protective effi
203 lity in order to identify optimal dosing for tuberculous meningitis.
204 ar stain improve the laboratory diagnosis of tuberculous meningitis.
205  or PCR (n = 2) and 11% (6/54) had confirmed tuberculous meningitis.
206  disease severity and outcome in adults with tuberculous meningitis.
207 HIV and 428 (85.8%) had definite or probable tuberculous meningitis.
208 ring a hospital admission, and in those with tuberculous meningitis.
209 ical impact of dexamethasone, as observed in tuberculous meningitis.
210 he new Xpert MTB/RIF Ultra (Xpert Ultra) for tuberculous meningitis.
211 as the initial diagnostic test for suspected tuberculous meningitis.
212 rt MTB/RIF as initial diagnostic testing for tuberculous meningitis.
213 sible tuberculous meningitis, and two as not tuberculous meningitis.
214 estions concerning the optimal management of tuberculous meningitis; these studies also form a platfo
215 imated to be in children who did not receive tuberculous-meningitis treatment.
216 ct of PDE-Is on the duration of treatment in tuberculous mice.
217  cilomilast accelerated the time to death in tuberculous mice.
218 finding that sequences representative of non-tuberculous mycobacteria (NTM) and other opportunistic h
219                                          Non-tuberculous mycobacteria (NTM) are a large family of aci
220 drug-resistant tuberculosis (MDR-TB) and non-tuberculous mycobacteria (NTM) infection, which can be u
221            The frequency of isolation of non-tuberculous mycobacteria (NTM) species from respiratory
222          Humans are regularly exposed to non-tuberculous mycobacteria (NTM) that live in soil and wat
223 teria, the four-gene module occurred only in tuberculous mycobacteria and was required for intramacro
224                                          Non-tuberculous mycobacteria cause a broad range of clinical
225 itive diagnostic assays for the detection of tuberculous mycobacteria in elephants are lacking.
226 ence of tuberculosis and infections with non-tuberculous mycobacteria in human populations, but the m
227 ie severe disease caused by environmental or tuberculous mycobacteria, and other intra-macrophagic mi
228                   Despite concerns about non-tuberculous mycobacteria, especially Mycobacterium absce
229 s mycobacterial populations with various non-tuberculous mycobacteria, including members of the Mycob
230 cid biosynthesis, is very potent against the tuberculous mycobacteria.
231                                Pulmonary non-tuberculous mycobacterial (NTM) disease epidemiology in
232          Furthermore, isolated pulmonary non-tuberculous mycobacterial infection has been increasing
233 to confer susceptibility to disseminated non-tuberculous mycobacterial infection.
234                   Cultures suggestive of Non-tuberculous mycobacterial infections (NTM) were sub-cult
235 actors underlying localised and systemic non-tuberculous mycobacterial infections.
236 th respiratory isolates met criteria for non-tuberculous mycobacterial pulmonary disease (NTM-PD).
237 ng infected with the multidrug-resistant non-tuberculous mycobacterium (NTM) Mycobacterium abscessus,
238 ium abscessus (Mab) is a rapidly growing non-tuberculous mycobacterium (NTM) that causes a wide range
239 s show promise as therapeutic agents for non-tuberculous mycobacterium infections.
240 scessus (Mab) is a highly drug-resistant non-tuberculous mycobacterium that presents major treatment
241 which has a smooth colony morphology, is the tuberculous organism retaining the most genetic traits f
242                    He found that children of tuberculous parents had higher mortality rates and lower
243  control tuberculosis, leprosy and other non-tuberculous pathogens.
244      To identify host cell genes involved in tuberculous pathology, we screened macrophage cDNA libra
245 d IL-1 beta, was not up-regulated in PBMC of tuberculous patients.
246 , NF-kappa B was activated in monocytes from tuberculous patients.
247  14 of 28 specimens (50%) from patients with tuberculous pericarditis (P > 0.15).
248 fluid (PF) lipoarabinomannan (LAM) assays in tuberculous pericarditis (TBP).
249               Sixteen of the 20 patients had tuberculous pericarditis and 4 patients had other diagno
250  30 of 43 specimens (70%) from patients with tuberculous pericarditis and by PCR in 14 of 28 specimen
251 ture and histopathology for the diagnosis of tuberculous pericarditis in 36 specimens of pericardial
252                                              Tuberculous pericarditis is associated with high morbidi
253 signed 1400 adults with definite or probable tuberculous pericarditis to either prednisolone or place
254                             In patients with tuberculous pericarditis, neither prednisolone nor M. in
255 le diseases such as rheumatic heart disease, tuberculous pericarditis, or cardiomyopathy and others h
256 ndicus pranii immunotherapy in patients with tuberculous pericarditis.
257 -characterized ascitic fluid bank, including tuberculous peritonitis (n = 7), tuberculous peritonitis
258  of ascitic fluid ADA activity in diagnosing tuberculous peritonitis in a U.S. patient population.
259 , including tuberculous peritonitis (n = 7), tuberculous peritonitis in the setting of cirrhosis (n =
260 ver, ADA was only 30% sensitive in detecting tuberculous peritonitis in the setting of cirrhosis, and
261 sis, and cirrhosis was present in 59% of the tuberculous peritonitis patients in our population.
262 ivity of the ADA determination in diagnosing tuberculous peritonitis was only 58.8%, and the specific
263                                              Tuberculous peritonitis, although common in Third World
264              We enrolled 91 cases, including tuberculous pleural effusion (TPE, n = 50), malignant pl
265 s facilitates monocyte transmigration during tuberculous pleural inflammation.
266 tributed, being more common in patients with tuberculous pleurisy (92%) in comparison with healthy M.
267 e pleural effusion, diagnostic treatment for tuberculous pleurisy by anti-tuberculosis drugs was perf
268                                              Tuberculous pleurisy is a severe inflammatory response i
269       Analysis of cytokine expression during tuberculous pleurisy may lead to a better understanding
270                                           In tuberculous pleurisy pleural mesothelial cells are expos
271         We have used the guinea pig model of tuberculous pleurisy to examine several aspects of the i
272 by using the established guinea pig model of tuberculous pleurisy.
273  in pleural biopsy sections of patients with tuberculous pleurisy.
274 cted of benign asbestos pleural effusion and tuberculous pleurisy.
275 f pleural macrophages in the pathogenesis of tuberculous pleuritis and to monitor the response to ant
276 hages play critical roles in pathogenesis of tuberculous pleuritis, but very little is known about th
277 l mesothelial cells (PMCs) express ICAM-1 in tuberculous pleuritis.
278 reater than those of PBMC from patients with tuberculous pleuritis.
279 owing antibiotics treatment in patients with tuberculous pleuritis.
280                                              Tuberculous pneumonia, necrotic granulomatous lesions, a
281 t mechanisms contribute to the prevention of tuberculous reactivation.
282 ry tuberculosis compared with those with non-tuberculous respiratory tract infections.
283 o be infected, with up to 8% having external tuberculous signs, in wild populations in Northumberland
284 diagnosed with pyogenic spondylodiscitis and tuberculous spondylodiscitis allowed identification of i
285 regarding possibility to distinguish between tuberculous spondylodiscitis and pyogenic spondylodiscit
286                       Prevailing features of tuberculous spondylodiscitis included: involvement of th
287                                              Tuberculous spondylodiscitis is characterized by the loc
288  with pyogenic spondylodiscitis, and 16 with tuberculous spondylodiscitis).
289                       Transient worsening of tuberculous symptomatology and lesions following antitub
290 okine that is implicated in the formation of tuberculous (TB) granulomas and in immunity to Mycobacte
291 R imaging allowed evaluation of all forms of tuberculous tenosynovitis (hygromatous, serofibrinous, a
292                                              Tuberculous tenosynovitis most commonly involved the ten
293                                 All cases of tuberculous tenosynovitis or bursitis showed soft-tissue
294                          Twelve patients had tuberculous tenosynovitis, and nine had bursitis.
295 osite reference standard of any positive CSF tuberculous test.
296                                Existing anti-tuberculous therapies require long treatments and are co
297 y more accurate in identifying true-positive tuberculous uveitis cases than was T-SPOT.TB among disco
298 and the tuberculin skin test) for diagnosing tuberculous uveitis.
299 red for assessment of the efficiency of anti-tuberculous vaccines.
300  meningitis (TBM) is the most severe form of tuberculous with substantial mortality.

 
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